ArticlePloS one2011
The menin tumor suppressor protein is phosphorylated in response to DNA damage.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Inhibition of SIRT7 Overcomes Radioresistance in Pancreatic Neuroendocrine Tumors by Reactivating MEN1 Expression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Extracellular signalling regulates gastrin transcription through site-specific phosphorylation and nuclear redistribution of Menin.bioRxiv : the preprint server for biology · 2026Article
- MEN1 is a regulator of alternative splicing and prevents R-loop-induced genome instability through suppression of RNA polymerase II elongation.Nucleic acids research · 2023Article
- Clinically Defined Mutations inCancer research communications · 2023Article
- Antisense Oligonucleotide-Based Therapeutic against Menin for Triple-Negative Breast Cancer Treatment.Biomedicines · 2021Article
- Multiple Endocrine Neoplasia Type 1: Latest Insights.Endocrine reviews · 2021Review
- Biomarkers for Pancreatic Neuroendocrine Neoplasms (PanNENs) Management-An Updated Review.Frontiers in oncology · 2020Review
- Article
- Genetics and Epigenetics of Gastroenteropancreatic Neuroendocrine Neoplasms.Endocrine reviews · 2019Review
- GLP-1 signaling suppresses menin's transcriptional block by phosphorylation in β cells.The Journal of cell biology · 2019Article
- Tissue-specific induced DNA methyltransferase 1 (Dnmt1) in endocrine pancreas by RCAS-TVA-based somatic gene transfer system promotes β-cell proliferation.Cancer gene therapy · 2019Article
- The Treatment Landscape and New Opportunities of Molecular Targeted Therapies in Gastroenteropancreatic Neuroendocrine Tumors.Targeted oncology · 2017Review
- Epigenetic regulation by the menin pathway.Endocrine-related cancer · 2017Review
- The future: genetics advances in MEN1 therapeutic approaches and management strategies.Endocrine-related cancer · 2017Review
- Loss of MEN1 activates DNMT1 implicating DNA hypermethylation as a driver of MEN1 tumorigenesis.Oncotarget · 2016Article
- Challenges and opportunities in targeting the menin-MLL interaction.Future medicinal chemistry · 2014Review
- Menin: a scaffold protein that controls gene expression and cell signaling.Trends in biochemical sciences · 2013Review
- MEN1 is a melanoma tumor suppressor that preserves genomic integrity by stimulating transcription of genes that promote homologous recombination-directed DNA repair.Molecular and cellular biology · 2013Article
- Menin mediates epigenetic regulation via histone H3 lysine 9 methylation.Cell death & disease · 2013Article
- SUMO modification of menin.American journal of cancer research · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMultiple endocrine neoplasia type 1 (MEN1) is a heritable cancer syndrome characterized by tumors of the pituitary, pancreas and parathyroid. Menin, the product of the MEN1 gene, is a tumor suppressor protein that functions in part through the regulation of transcription mediated by interactions with chromatin modifying enzymes. PRINCIPAL
findingsHere we show menin association with the 5' regions of DNA damage response genes increases after DNA damage and is correlated with RNA polymerase II association but not with changes in histone methylation. Furthermore, we were able to detect significant levels of menin at the 3' regions of CDKN1A and GADD45A under conditions of enhanced transcription following DNA damage. We also demonstrate that menin is specifically phosphorylated at Ser394 in response to several forms of DNA damage, Ser487 is dynamically phosphorylated and Ser543 is constitutively phosphorylated. Phosphorylation at these sites however does not influence the ability to interact with histone methyltransferase activity. In contrast, the interaction between menin and RNA polymerase II is influenced by phosphorylation, whereby a phospho-deficient mutant had a higher affinity for the elongating form of RNA polymerase compared to wild type. Additionally, a subset of MEN1-associated missense point mutants, fail to undergo DNA damage dependent phosphorylation.
conclusionTogether, our findings suggest that the menin tumor suppressor protein undergoes DNA damage induced phosphorylation and participates in the DNA damage transcriptional response.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.